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Srs2 helicase prevents the formation of toxic DNA damage during late prophase I of yeast meiosis
Bibliographic Information
- Published
- 2019-01-11
- Resource Type
- journal article
- DOI
-
- 10.1101/518035
- 10.1007/s00412-019-00709-5
- Publisher
- openRxiv
Search this article
Description
<jats:title>Abstract</jats:title> <jats:p> Proper repair of double-strand breaks (DSBs) is key to ensure proper chromosome segregation. In this study, we found that the deletion of the <jats:italic>SRS2</jats:italic> gene, which encodes a DNA helicase necessary for the control of homologous recombination, induces aberrant chromosome segregation during budding yeast meiosis. This abnormal chromosome segregation in <jats:italic>srs2</jats:italic> cells accompanies the formation of a novel DNA damage induced during late meiotic prophase-I. The damage may contain long stretches of single-stranded DNAs (ssDNAs), which lead to aggregate formation of a ssDNA binding protein, RPA, and a RecA homolog, Rad51, as well as other recombination proteins inside of the nuclei. The Rad51 aggregate formation in the <jats:italic>srs2</jats:italic> mutant depends on the initiation of meiotic recombination and occurs in the absence of chromosome segregation. Importantly, as an early recombination intermediate, we detected a thin bridge of Rad51 between two Rad51 foci or among the foci in the <jats:italic>srs2</jats:italic> mutant, which is rarely seen in wild type. These might be cytological manifestation of the connection of two DSB ends and multi-invasion. The DNA damage with Rad51 aggregates in the <jats:italic>srs2</jats:italic> mutant is passed through anaphase-I and -II, suggesting the absence of DNA damage-induced cell-cycle arrest after the pachytene stage. We propose that Srs2 helicase resolves early protein-DNA recombination intermediates to suppress the formation of aberrant lethal DNA damage during late prophase-I. </jats:p>
Journal
-
- Chromosoma
-
Chromosoma 128 (3), 453-471, 2019-01-11
openRxiv
